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Conference Paper: Genetic deletion of aldose reductase protects the neonatal mouse retina from oxygen-induced retinopathy

TitleGenetic deletion of aldose reductase protects the neonatal mouse retina from oxygen-induced retinopathy
Authors
Keywords703 retinopathy of prematurity
416 amacrine cells
602 Muller cells
Issue Date2010
PublisherARVO.
Citation
The 2010 Annual Meeting of the Association for Research in Vision and Ophthalmology (ARVO), Fort Lauderdale, FL., 2-6 May 2010. How to Cite?
AbstractPURPOSE: Retinopathy of prematurity (ROP) is a common retinal disease that occurs in premature babies with initial vessel loss followed by vessel proliferation. Oxidative stress and retinal dysfunction has been reported. We previously showed that genetic deletion or pharmacological inhibition of aldose reductase (AR), a rate limiting enzyme in polyol pathway, prevented RGC loss and oxidative stress after retinal ischemia/reperfusion injury (Cheung et al Exp Eye Res 2007 85:608). Here, we assessed the effects of aldose reductase deletion on retinal injury induced by hyperoxic exposure using a mouse model of ROP. METHODS: Seven-day-old pups (P7) were exposed to 75% oxygen for 5 days and then returned to room air environment for 5 days. Vessel architecture and neuronal responses after hyperoxia were examined and compared between wild-type and AR-deficient retinae. Immunohistochemistry for immunoglobulin G (IgG), calretinin, glial fibrillary acidic protein (GFAP), nitrotyrosine (NT), inducible nitric oxide synthase (iNOS) were performed. RESULTS: At P12 (immediately after hyperoxia), AR-deficient retina displayed significantly smaller central avascular area (57.9±1.1% vs. 64.3±1.4% in wild-type retina, p<0.003). There was significant reduction in thickness of central INL and entire IPL in wild-type retina but not in AR-deficient retina (p<0.05). GFAP immunoreactivity was increased and the intensity was stronger in AR-deficient retina, but that for calretinin in wild-type and AR-deficient retinae was similar. At P17 (5 days after hyperoxia), central avascular area persisted in wild-type retina (24.8±1.7%). Again, AR-deficient retina showed a smaller area (16.1±1.2%, p<0.0005). Interestingly, blood vessels along GCL of wild-type retina displayed IgG extravasation after hyperoxia. Yet, this was much reduced in AR-deficient retina. There was absence of calretinin staining in INL together with seriously distorted strata in IPL of wild-type retina but not AR-deficient retina. Increased intense GFAP staining was seen in central-middle retina of wild-type but not AR-deficient mice. Increased NT immunoreactivity was found in INL of wild-type retina but this increase was less apparent in AR-deficient retina. Similar increase in iNOS immunostaining was observed in wild-type and AR-deficient retina. CONCLUSION: Our observations indicated that AR deletion reduced avascular area, IgG leakage, amacrine cell loss, and NT induction upon hyperoxia, suggesting a protective role of AR deficiency in ROP.
DescriptionProgram#/Poster#: 4465/A398
Poster Session no. 451 - Oxygen-induced Retinopathy
Persistent Identifierhttp://hdl.handle.net/10722/127947

 

DC FieldValueLanguage
dc.contributor.authorLo, ACYen_HK
dc.contributor.authorFu, Zen_HK
dc.contributor.authorLi, SYen_HK
dc.contributor.authorWong, Den_HK
dc.contributor.authorChung, SKen_HK
dc.date.accessioned2010-10-31T13:55:58Z-
dc.date.available2010-10-31T13:55:58Z-
dc.date.issued2010en_HK
dc.identifier.citationThe 2010 Annual Meeting of the Association for Research in Vision and Ophthalmology (ARVO), Fort Lauderdale, FL., 2-6 May 2010.en_HK
dc.identifier.urihttp://hdl.handle.net/10722/127947-
dc.descriptionProgram#/Poster#: 4465/A398-
dc.descriptionPoster Session no. 451 - Oxygen-induced Retinopathy-
dc.description.abstractPURPOSE: Retinopathy of prematurity (ROP) is a common retinal disease that occurs in premature babies with initial vessel loss followed by vessel proliferation. Oxidative stress and retinal dysfunction has been reported. We previously showed that genetic deletion or pharmacological inhibition of aldose reductase (AR), a rate limiting enzyme in polyol pathway, prevented RGC loss and oxidative stress after retinal ischemia/reperfusion injury (Cheung et al Exp Eye Res 2007 85:608). Here, we assessed the effects of aldose reductase deletion on retinal injury induced by hyperoxic exposure using a mouse model of ROP. METHODS: Seven-day-old pups (P7) were exposed to 75% oxygen for 5 days and then returned to room air environment for 5 days. Vessel architecture and neuronal responses after hyperoxia were examined and compared between wild-type and AR-deficient retinae. Immunohistochemistry for immunoglobulin G (IgG), calretinin, glial fibrillary acidic protein (GFAP), nitrotyrosine (NT), inducible nitric oxide synthase (iNOS) were performed. RESULTS: At P12 (immediately after hyperoxia), AR-deficient retina displayed significantly smaller central avascular area (57.9±1.1% vs. 64.3±1.4% in wild-type retina, p<0.003). There was significant reduction in thickness of central INL and entire IPL in wild-type retina but not in AR-deficient retina (p<0.05). GFAP immunoreactivity was increased and the intensity was stronger in AR-deficient retina, but that for calretinin in wild-type and AR-deficient retinae was similar. At P17 (5 days after hyperoxia), central avascular area persisted in wild-type retina (24.8±1.7%). Again, AR-deficient retina showed a smaller area (16.1±1.2%, p<0.0005). Interestingly, blood vessels along GCL of wild-type retina displayed IgG extravasation after hyperoxia. Yet, this was much reduced in AR-deficient retina. There was absence of calretinin staining in INL together with seriously distorted strata in IPL of wild-type retina but not AR-deficient retina. Increased intense GFAP staining was seen in central-middle retina of wild-type but not AR-deficient mice. Increased NT immunoreactivity was found in INL of wild-type retina but this increase was less apparent in AR-deficient retina. Similar increase in iNOS immunostaining was observed in wild-type and AR-deficient retina. CONCLUSION: Our observations indicated that AR deletion reduced avascular area, IgG leakage, amacrine cell loss, and NT induction upon hyperoxia, suggesting a protective role of AR deficiency in ROP.-
dc.languageengen_HK
dc.publisherARVO.-
dc.relation.ispartofARVO 2010 Annual Meeting-
dc.subject703 retinopathy of prematurity-
dc.subject416 amacrine cells-
dc.subject602 Muller cells-
dc.titleGenetic deletion of aldose reductase protects the neonatal mouse retina from oxygen-induced retinopathyen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailLo, ACY: amylo@hku.hken_HK
dc.identifier.emailLi, SY: sukyeeli@hku.hken_HK
dc.identifier.emailWong, D: shdwong@hku.hken_HK
dc.identifier.emailChung, SK: skchung@hkucc.hku.hken_HK
dc.identifier.authorityLo, ACY=rp00425en_HK
dc.identifier.authorityWong, D=rp00516en_HK
dc.identifier.authorityChung, SK=rp00381en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros181392en_HK
dc.publisher.placeUnited States-

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